Skeletal muscle plays an integral role in the regulation of the circulating glucose concentration. Thus, the mechanism for skeletal muscle insulin resistance is of great importance for the understanding of the pathogenesis of type-2 diabetes. While a great deal of research has been done on determining what causes skeletal muscle insulin resistance, the mechanism remains unclear. Recent work has suggested that reduced mitochondrial content and/or function in skeletal muscle contributes to insulin resistance and may in fact be genetically determined. It is our hypothesis that the reduction in muscle mitochondria is due to physical inactivity and plays no role in modulating muscle insulin resistance. The primary goal of this study determine the effect of a high fat diet that causes visceral obesity and insulin resistance on skeletal muscle content and functional mitochondria in rats. A second goal is to determine whether insulin stimulated phospohorylation of Akt substrate 160 is impaired in response to high fat feeding. [unreadable] [unreadable] [unreadable]